Download Regulation of blood glucose

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1.6
Regulation of blood glucose
The pancreas, and control of blood glucose concentration, insulin and glucagon
The pancreas
The pancreas is an organ which is both an endocrine gland and an exocrine gland, as it has functions of both types. The
majority of cells in the pancreas have an exocrine function, in secreting digestive enzymes. Such cells are found
surrounding tiny tubules into which they secrete pancreatic juice, a liquid containing a number of digestive enzymes, and
the tubes will join up at the pancreatic duct which carries the pancreatic juice into the first section of the small intestine.
The pancreatic juice includes the enzymes amylase, pancreatic lipase, carboxypeptidase, elastase and trypsinogen.
liver
stomach
gall bladder
to heart
and rest of
the body
bile duct
islet of Langerhans
cells secrete insulin or
glucagon into blood
pancreas
blood with
hormones
returned to
circulation
Small areas in the pancreas called
islets of Langerhans consist of two
types of cell. There are the α-cells
which manufacture and secrete the
hormone glucagon, and there are βcells which manufacture and secrete
the hormone insulin. The islets are
well supplied with blood capillaries
and the hormones are secreted
directly into the blood.
islet of
Langerhans cell
capillary
food passing
through small
intestine
pancreatic duct carries pancreatic cells
pancreatic juice to
secrete pancreatic
small intestine
juice which drains to
the duct
secretion of
pancreatic
juice into
small intestine
small intestine
pancreatic
cells
vein
Regulating blood glucose levels
It is the role of the cells in the islets of Langerhans to monitor the concentration of blood glucose. If they detect a
concentration which lies outside the acceptable range, the appropriate cells (either α-cells or β-cells) are activated to
release hormones to respond and return the blood glucose concentration to an acceptable level.
increase in glucose
concentration
Detected by
β-cells in islet of
Langerhans
β-cells secrete
insulin into the
bloodstream
hepatocytes
respond to
hormone
level of
respiration
increases
Normal blood
glucose level
decrease in glucose
concentration
decrease in glucose
concentration
Normal blood
glucose level
Detected by
α-cells in islet of
Langerhans
α-cells secrete
glucagon into the
bloodstream
hepatocytes
respond to
hormone
breakdown of
glucose and
fatty acids
increase in glucose
concentration
The diagram above shows how the cells in the islet of Langerhans help to maintain a regular blood glucose concentration.
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A rise in blood glucose concentration
When blood glucose levels increase, possibly just after eating a meal, the change in concentration is detected by β-cells in
the islets of Langerhans. The cells then secrete the hormone insulin directly into the bloodstream. Insulin, like adrenaline,
has a number of effects on multiple cell types around the body. The target cells for insulin are the hepatocytes (liver cells)
as well as muscle cells. The diagram shows insulin secretion:
2 when there is a
concentration gradient,
glucose diffuses into the
cell via facilitated diffusion
1 under normal conditions
potassium ions flow out of
the cell
3 glucose is respired
and ATP produced
ADP + Pi
2+
8 Ca enters the cell
and bind to vesicles
containing insulin,
causing them to fuse
with the membrane
4 ATP binds to
+
the K channels
to close them
ATP
+
5 K ions
remain in the
cell because of
the closed
channels
7 change in potential difference
causes voltage-gated calcium ion
channels to open
6 accumulation of K
increases potential
difference of the
membrane
+
+
In the resting β-cell, potassium ions (K ) are moving out of the cell down the concentration gradient, via facilitated
diffusion. When there is a concentration of glucose from outside the cell to inside the cell, for example, after eating,
glucose enters the cell through specialised glucose channels in the membrane (again, by facilitated diffusion). The glucose
inside the cell is then respired, producing ATP.
The ATP moves to the potassium ion channels on the cell surface membrane, and binds to the channels, causing them to
close. This means that the potassium ions stay inside of the cell. Quickly, the build up of the ions depolarises the
2+
membrane (it becomes less negative), causing the voltage-gated calcium ion (Ca ) channels to open, which results in an
influx of calcium ions into the cell. These ions then bind to vesicles within the cell which carry the insulin hormones. The
calcium causes the vesicles to move to the cell surface membrane, and undergo exocytosis: the vesicle fuses with the
membrane and the insulin is released out of the cell, and into the bloodstream.
When insulin is released into the blood, it is transported all around the body, and when it passes the target tissues
(mainly the hepatocytes), the hormone binds to the receptor sites, activating the adenyl cyclase enzyme on the inner cell
membrane. This produces cyclic AMP (cAMP) from a molecule of ATP, and the cyclic AMP activates a number of
intracellular reactions. The effects of the hormone insulin, or these end intracellular reactions, are:
 more glucose channels are inserted into the cell surface membrane, so that more glucose can enter the cell
 glucose inside the cell is polymerised into glycogen by a process known as glycogenesis
 more glucose is converted into fats, and more glucose is respired
Needless to say, as these events cause more and more glucose to enter the target cells, the result is a decreased glucose
concentration in the bloodstream. The concentration returns to an acceptable level using this process.
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A drop in blood glucose concentration
An example of an activity that would cause a fall in blood glucose level is after exercise. The drop in glucose concentration
in the bloodstream is detected by α-cells in the islets of Langerhans. In response to this, the α-cells will secrete the
hormone glucagon, which again uses the hepatocytes as target cells.
When glucagon is released, it binds to the receptors on its target cells. This activates the adenyl cyclase, stimulating the
production of cAMP, which will be the eventual trigger for the reactions. The effects of glucagon are:
 the polymer glycogen is broken down into the monomer glucose, this process is called glycogenolysis
 more fatty acids are used in respiration
 amino acids and lipids are converted into glucose by a process known as gluconeogenesis
The effects of glycogenolysis and gluconeogenesis (breakdown of glycogen and conversion of non-sugars into glucose)
results in the release of much glucose into the blood, restoring it to an acceptable level.
Diabetes
Diabetes mellitus is a disease where the body is no longer able to maintain an acceptable blood glucose concentration,
and is described as a lack of control over blood glucose regulation. It can lead to hyperglycaemia (very high levels of
blood glucose) after a meal rich in sugars, and also hypoglycaemia (very low levels) after exercise.
Type I diabetes
Also known as insulin dependent diabetes, type I diabetes is early-onset, meaning it occurs from when the sufferer is very
young. It is an auto-immune disease, where the body’s own cells destroy the insulin-releasing β-cells, and so the effect is
that little or no insulin is released, which can lead to hyperglycaemia, for example after eating a meal.
The treatment for type I diabetes is using insulin injections. Precise dosages of insulin to counteract food eaten is injected.
The necessary dosage is calculated by measuring blood glucose levels using a pin-prick. Originally, the insulin to be
injected was obtained from the pancreas of pigs. This was because it was fairly similar to humans’ insulin and easy to rear,
although there were some problems, including low extraction efficiency, a risk of the immune system rejecting the pig
insulin, and not to mention the moral and ethical issues.
Ergo the more modern treatment which uses injections of insulin produced by genetically-modified bacteria. Larger
quantities can be produced in batches more easily and quickly in this method, and the chances of rejection by the
immune system are far slimmer, as human DNA coding is used in the genetic modification (restriction enzymes cut out
the DNA coding for insulin production, and other enzymes place that coding into the bacteria, which reproduces over
time). There are obviously fewer ethical issues concerning artificial insulin production. This insulin is closer to human
insulin, also, and so it is more likely to bind to the receptor sites on hepatocytes than pig insulin is.
Type II diabetes
Described as non-insulin dependent or late-onset diabetes, type II diabetes is not due to problems with β-cells, but the
problem lies with the not-functioning receptors in the hepatocytes. People with type II diabetes can still manufacture and
release insulin, but certain factors will reduce the responsiveness to the hormone over time. The most common factor is
age: as people grow older, they become less reactive to the hormone, and so insulin doesn’t bind to the target tissues as
readily. But other factors can result in an earlier onset of this type of diabetes, including obesity, diets high in sugars, race
(Asian and Afro-Caribbean people are less responsive to insulin) and family history.
The treatment of type II diabetes is simply monitoring lifestyle. Regular exercise and a healthy diet are the best ways to
reduce the chance of developing late-onset diabetes.
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